BUB1 promotes proliferation of liver cancer cells by activating SMAD2 phosphorylation
- Li‑Jing Zhu
- Yan Pan
- Xiao‑Ying Chen
- Pan‑Fei Hou
Affiliations: Department of Radiation Oncology, Lianshui County People's Hospital, Huaian, Jiangsu 223400, P.R. China, Department of Clinical Laboratory, Lianshui County People's Hospital, Huaian, Jiangsu 223400, P.R. China, Clinical Laboratory, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China
- Published online on: March 5, 2020 https://doi.org/10.3892/ol.2020.11445
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Budding uninhibited by benzimidazoles 1 (BUB1) is a mitotic checkpoint serine/threonine kinase that has been reported as an oncogene or tumor suppressor gene in various types of cancer, including breast cancer, pancreatic ductal adenocarcinoma, prostate and gastric cancers. However, its role in liver cancer remains unclear. The present study aimed to explore the biological function of BUB1 in liver cancer. The present study demonstrated that BUB1 mRNA expression levels and the intensity of immunohistochemical staining were significantly increased in liver cancer tissues compared with normal tissues. The role of BUB1 in cell proliferation was also determined. Overexpression of BUB1 significantly promoted cell proliferation, whereas knockdown of BUB1 expression inhibited the proliferation of liver cancer cell lines. In experiments investigating the underlying mechanism, overexpression of BUB1 increased the levels of SMAD2 phosphorylation, whereas knockdown of BUB1 reduced the levels of SMAD2 phosphorylation. Therefore, BUB1 may promote proliferation of liver cancer cells by activating phosphorylation of SMAD2, and BUB1 may serve as a potential target in the diagnosis and/or treatment of liver cancer.